Another major parallel between the human and monkey data has been the finding that, as in humans, the stress-related S allele phenotype in monkeys is related to an intermediate neural phenotype characterized by abnormal corticolimbic structure and function. For example, the S allele in monkeys also has been mapped onto reduced gray matter volumes in the amygdala, medial prefrontal and orbitofrontal cortex, and pulvinar (88). Moreover, monkeys with the S allele exhibit greater metabolic activity than LL homozygotes in the amygdala and its networked cortical regions, including orbitofrontal cortex, in response to the stress of relocation (89). Given the importance of the orbitofrontal cortex in social behavior, abnormalities in this region might also account for the finding that S-carriers engage in less eye gaze with high status conspecifics and are more risk-averse in their presence (90). An intriguing development is recent data from S-carrier monkeys (88) and 5-HTT mutant mice (91) demonstrating that reversal learning, a measure of cognitive flexibility subserved by the orbitofrontal cortex (92), is enhanced as a function of relative 5-HTT gene deficiency. This may reflect increased
